We have learned from our previous experiments that ablation of the peripheral sympathetic nervous system profoundly influences immune responses, changes the proportions of the lymphocyte subsets, and increases the number of Beta-adrenergic receptors on the lymphocyte surface. We now plan to study the significance of the autonomic nervous system in the pathogenesis of autoimmune diseases. We will study experimental autoimmune myasthenia gravis which will serve as a model for antibody-mediated autoimmune diseases and as an experimental model for human myasthenia gravis. We will also study experimental allergic encephalomyelitis which is a model for cell-mediated autoimmune diseases and is commonly used as a possible model for multiple sclerosis. Using flow cytometry, we will continue to study functional changes in lymphocytes from animals with a destroyed sympathetic nervous system and will compare the changes observed with functional changes observed in lymphocytes from mice with an hypertrophied sympathetic nervous system. We believe that an understanding of how the sympathetic nervous system interacts with the nervous system and how it influences autoimmune diseases will have an impact on the prevention and treatment of these diseases.